6533b83afe1ef96bd12a794b
RESEARCH PRODUCT
Alpha 2-receptor-mediated inhibition of intraluminal release of gastric somatostatin in anaesthetized rats.
D. GarciaSalvador F. AliñoKerstin Uvnäs-mobergsubject
Malemedicine.medical_specialtySympathetic Nervous SystemPhysiologyNeuropeptideClonidinePhentolamineInternal medicineGastrinsmedicineAnimalsAnesthesiaPhentolamineGastrinbusiness.industryStomachdigestive oral and skin physiologyRats Inbred StrainsVagus NerveHydrogen-Ion ConcentrationReceptors Adrenergic alphaElectric StimulationVagus nerveRatsEndocrinologymedicine.anatomical_structureSomatostatinGastrointestinal hormoneGastric MucosabusinessSomatostatinPerfusionhormones hormone substitutes and hormone antagonistsmedicine.drugdescription
Alino, S. F., Garcia, D. & Uvnas-Moberg, K. 1992. Alpha2-receptor-mediated inhibition of intraluminal release of gastric somatostatin in anaesthetized rats. Acta Physiol Scand144, 233–238. Received 22 February 1991, accepted 11 October 1991. ISSN 00014772. Department of Pharmacology and Pharmaceutics, University of Valencia, Valencia, Spain, Department of Cell Biology and Morphology Science, University of Pais Vasco, Leioa, Spain and Department of Pharmacology, Karolinska Institute, Stockholm, Sweden. The aim of the present study was to investigate how the sympathetic nervous system affects the vagally induced intragastric release of somatostatin and gastrin. Experiments were performed on anaesthetized rats in which the stomach was perfused with a dextrane solution (pH ≅ 5.9) or dextrane buffer (pH 7.4). pH as well as gastrin and somatostatin levels were measured in the gastric perfusate when it had passed the stomach. Vagal stimulation caused a decrease in perfusate pH and an increase of the intraluminal output of gastrin and somatostatin when the stomach was perfused with the dextrane solution pH 5.9. Pretreatment with phentolamine (1 mg kg-1) significantly increased and pretreatment with clonidine (60, ug kg-1 h-1) significantly decreased somatostatin release caused by vagal stimulation, whereas gastrin levels remained largely unchanged. The effect of clonidine persisted in rats pretreated with indomethacin (5 mg kg-1), which per se potentiates the vagally induced luminal somatostatin release. When the stomach was perfused with the dextrane buffer pH 7.4, basal gastrin levels were significantly higher than during perfusion with the solution pH 5.9, whereas somatostatin levels remained unchanged. Neither somatostatin nor gastrin levels increased following vagal stimulation during gastric perfusion with the dextrane buffer pH 7.4. However, following pretreatment with phentolamine somatostatin levels increased during these conditions.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 1992-03-01 | Acta physiologica Scandinavica |